Publication:
Nesfatin-1 ameliorates testicular injury and supports gonadal function in rats induced with testis torsion

dc.contributor.authorYILDIRIM, ALPER
dc.contributor.authorsTamer, Sevil Arabaci; Yildirim, Alper; Koroglu, M. Kutay; Cevik, Ozge; Ercan, Feriha; Yegen, Berrak C.
dc.date.accessioned2022-03-12T22:25:23Z
dc.date.available2022-03-12T22:25:23Z
dc.date.issued2018
dc.description.abstractTesticular torsion causes ischemia-reperfusion injury and an increased risk of infertility. Nesfatin-1 is a novel peptide with antioxidant, anti-inflammatory and anti-apoptotic properties. In the present study, we aimed to investigate the putative beneficial effects of nesfatin-1 on oxidative injury and impaired testicular function induced by testis torsion. Under anesthesia, male Sprague-Dawley rats (180-230 g; n = 24) had sham-operation or they underwent testicular torsion by rotating the left testis 720 degrees and fixing it for 2 h, followed by a 2-h detorsion. Rats in each group were treated intraperitoneally with either nesfatin-1 (0.3 mu g/kg) or saline prior to the torsion or sham-torsion. At the end of the 4-h experimental period, tissue samples were removed for evaluation of spermatozoa, molecular and histochemical analyses. In saline-treated torsion/detorsion group, a high percentage of abnormal spermatozoa with head defects was observed, which was abolished in nesfatin-1 -treated torsion/detorsion group. The levels of 8-OHdG, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, caspase-3 were increased in the saline-treated torsion/detorsion group as compared to sham-operated group, while nesfatin-1 pre-treatment significantly decreased the expressions of the pro-inflammatory cytokines, depressed apoptosis, and also reduced the tubular degeneration. In addition, nesfatin-1 in torsion/detorsion group elevated expressions of transforming growth factor (TGF)-beta and reduced expressions of protein kinase B (AKT) and cAMP response element binding protein (CREB) in the testis tissue. The present findings show that nesfatin-1, by regulating AKT and CREB signaling pathways and pro-inflammatory/anti-inflammatory cytokine balance, preserves the spermatogenic cells and ameliorates torsion-detorsion-induced tubular degeneration.
dc.identifier.doi10.1016/j.peptides.2018.07.005
dc.identifier.eissn1873-5169
dc.identifier.issn0196-9781
dc.identifier.pubmed30031042
dc.identifier.urihttps://hdl.handle.net/11424/234913
dc.identifier.wosWOS:000443255400001
dc.language.isoeng
dc.publisherELSEVIER SCIENCE INC
dc.relation.ispartofPEPTIDES
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectTestis torsion
dc.subjectApoptosis
dc.subjectOxidative stress
dc.subjectSpermatogenesis
dc.subjectNesfatin-1
dc.subjectCytokines
dc.subjectISCHEMIA-REPERFUSION INJURY
dc.subjectGERM-CELL APOPTOSIS
dc.subjectISCHAEMIA/REPERFUSION INJURY
dc.subjectPROINFLAMMATORY CYTOKINES
dc.subjectANDROGEN RECEPTOR
dc.subjectOXIDATIVE STRESS
dc.subjectACTIVATION
dc.subjectEXPRESSION
dc.subjectDAMAGE
dc.subjectPATHWAY
dc.titleNesfatin-1 ameliorates testicular injury and supports gonadal function in rats induced with testis torsion
dc.typearticle
dspace.entity.typePublication
local.avesis.id333cf2d4-beb8-448d-91eb-606970e8daac
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages9
local.journal.quartileQ2
oaire.citation.endPage9
oaire.citation.startPage1
oaire.citation.titlePEPTIDES
oaire.citation.volume107
relation.isAuthorOfPublication1840e6a0-5ec8-42b9-bca3-4e891749ac77
relation.isAuthorOfPublication.latestForDiscovery1840e6a0-5ec8-42b9-bca3-4e891749ac77

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